The pathophysiological mechanisms behind this process are intensively studied. In vitro studies show that elevated phosphate concentrations induce differentiation of vascular smooth muscle cells (VSMC) via Cbfa1 to osteoblast-like cells. These osteoblast-like cells are capable of producing bone matrix proteins, which may subsequently regulate mineralization. Once mineralization is initiated, increased Ca x PO4 product from (ab)normal bone metabolism, secondary hyperparathyroidism, or excessive calcium intake may accelerate this process leading to vascular calcification.